The cl2/dro1/ccdc80 null mice develop thyroid and ovarian neoplasias

Giovanni Scambia, Vincenza Leone, Angelo Ferraro, Filippo Schepis, Antonella Federico, Romina Sepe, Claudio Arra, Concetta Langella, Giuseppe Palma, Carlo De Lorenzo, Giancarlo Troncone, Alfredo Fusco, Pierlorenzo Pallante

Risultato della ricerca: Contributo in rivistaArticolo in rivista

7 Citazioni (Scopus)


We have previously reported that the expression of the CL2/CCDC80 gene is downregulated in human papillary thyroid carcinomas, particularly in follicular variants. We have also reported that the restoration of CL2/CCDC80 expression reverted the malignant phenotype of thyroid carcinoma cell lines and that CL2/CCDC80 positively regulated E-cadherin expression, an ability that likely accounts for the role of the CL2/CCDC80 gene in thyroid cancer progression. In order to validate the tumour suppressor role of the CL2/CCDC80 gene in thyroid carcinogenesis we generated cl2/ccdc80 knock-out mice. We found that embryonic fibroblasts from cl2/ccdc80(-/-) mice showed higher proliferation rate and lower susceptibility to apoptosis. Furthermore, cl2/ccdc80(-/-) mice developed thyroid adenomas and ovarian carcinomas. Finally, ret/PTC1 transgenic mice crossed with the cl2/ccdc80 knock-out mice developed more aggressive thyroid carcinomas compared with those observed in the single ret/PTC1 transgenic mice. Together, these results indicate CL2/CCDC80 as a putative tumour suppressor gene in human thyroid carcinogenesis.
Lingua originaleEnglish
pagine (da-a)535-541
Numero di pagine7
RivistaCancer Letters
Stato di pubblicazionePubblicato - 2015


  • cl2/dro1/ccdc80
  • thyroid and ovarian neoplasias

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